Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection

The present study investigated whether heat stress-induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2-terminal kinase (JNK) activation during ischaemia-reperfusion in a model of isolated perfused rat heart. Wistar rats were subjected to whole-body hyperthermia at 42degreesC for 15 min (HS), while untreated animals served as controls (CON). Twenty four hours later, CON and HS isolated hearts were perfused in a Langendorff mode and subjected to 20 min of zero-flow global ischaemia followed by 45 min of reperfusion. Postischaemic recovery of left ventricular developed pressure at 45 min of reperfusion was expressed as % of the initial value (LVDP%). Activation of p38 MAPK and JNK was assessed by standard Western blotting techniques using a dual phospho-p38 MAPK and phospho-p46 JNK and p54 JNK antibodies. The levels of phospho-p38 MAPK at the end of reperfusion were not different in HS as compared to CON hearts. The levels of phospho-p46. JNK and p54 JNK were 1.4- and 1.6-fold less in HS than in CON hearts respectively, p < 0.05. LVDP% was 60.3 (s.e.m., 6.3) for HS and 42.9 (4.1) for CON, p < 0.05. In summary, beat stress pretreatment improves postischaemic recovery of function in isolated rat hearts and this is associated with sup. pressed JNK activation in response to ischaemia-reperfusion.